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目的:研究三氧化二砷对多药耐药急性白血病细胞株K562/A02凋亡与细胞周期的影响及可能机制。方法:取阿霉素(Adr)的耐药白血病细胞株分为未加药的对照组及加入不同浓度的三氧化二砷(其终浓度为4.0μmol/L、5.0μmol/L)组,流式细胞仪检测细胞凋亡及细胞周期分布,Western blot方法检测不同浓度三氧化二砷对K562/A02细胞核NF-κBp65蛋白水平。结果:与对照组比较,三氧化二砷可显著增加Adr对K562/A02细胞凋亡率,阻滞细胞于G0/G1期,降低K562/A02细胞胞核中NF-kB p65的表达(P均<0.05)。结论:三氧化二砷可能是通过抑制NF-kB的胞内活化转位,从而促进K562/A02细胞凋亡及抑制细胞增殖。
Aims: To investigate the effects of arsenic trioxide on the apoptosis and cell cycle of multidrug resistant acute leukemia K562 / A02 cells and its possible mechanism. Methods: The adriamycin-resistant leukemia cell lines were divided into untreated control group and different concentrations of arsenic trioxide (final concentrations 4.0 micromol / L, 5.0 micromol / L). Flow cytometry Apoptosis and cell cycle distribution were detected by Western blot. The levels of NF-κB p65 protein in K562 / A02 cells were detected by different concentrations of arsenic trioxide. Results: Compared with the control group, arsenic trioxide could significantly increase the apoptosis rate of K562 / A02 cells, arrest the cells in the G0 / G1 phase and decrease the expression of NF-κB p65 in K562 / A02 cells (all P <0.05) . Conclusion: Arsenic trioxide may promote the apoptosis of K562 / A02 cells and inhibit cell proliferation by inhibiting the intracellular activation of NF-kB.